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| chemicals produced by microorganisms that inhibit or destroy other microorganisms |
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| chemicals synthesized artificially (in the laboratory) that inhibit or destroy microorganisms |
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| synthetic antimicrobial chemicals that are derivatives (modifications) of natural antibiotics. |
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| first systematic attempt to identify chemicals for the treatment of infectious diseases; he discovered Salvarsan, which is used to treat syphilis. |
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| : developed the use of sulfa drugs to target pathogens and treat infectious disease. |
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| discovered the antibiotic penicillin in cultures contaminated with the molds Penicillium notatum and Penicillium chrysogenum. |
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| Drug Mechanisms of Action |
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Definition
Inhibition of Cell Wall Synthesis Disruption of Cell Membrane Function Inhibition of Protein Synthesis Inhibition of Nucleic Acid Synthesis (DNA or RNA) Action as Antimetabolites (molecular mimicry) |
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| Two Examples of Antimetabolites (molecular mimicry) |
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| Sulfanilamide (a sulfa drug) and para-aminosalicylic |
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| Side effects of chemotheraputic drugs |
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Host Toxicity Allergic Response Disruption of normal flora |
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| occurs when a DNA mutation alters the target of an antibiotic sufficiently to remove its effectiveness. For example, mutations that alter ribosomes can confer resistance to antibiotics that inhibit protein synthesis. |
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| Extrachromosomal resistance |
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| usually due to the presence or acquisition of R plasmids, which are plasmids that contain up to seven resistance (R) genes, each of which confers resistance to a different antibiotic. |
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| Mutations in target molecules |
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| Quinolones may be rendered useless if the target, DNA gyrase, is modified by mutation. |
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| Alterations in membrane permeability |
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Definition
| The drug must be able to enter the cell to be effective. In addition, some microorganisms have special transport proteins that actively pump out antibiotics that have entered the cell. |
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| Some pathogens have enzymes that digest (break down) antibiotics. For example, β-lactamase destroys β-lactam drugs, such as penicillins. |
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Mutations can result in enzymes that have a reduced affinity for antimetabolites. For example, sulfonamide-resistant bacteria have an altered enzyme that has a very high affinity for PABA and a greatly reduced affinity for sulfonamide. |
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| Alterations in Anabolic Pathways |
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Definition
Drugs that disrupt metabolic pathways lose their effectiveness if bacteria develop new ways to acquire metabolites. For example, the folic acid synthesis pathway inhibited by sulfa drugs has become unnecessary for bacteria that have developed a mechanism to import pre-formed folic acid from their environment. |
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| First/Second/Third Line Drugs |
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Definition
If resistance to an initial drug used to treat a disease develops, then a second drug that effectively treats the disease must be found. If resistance develops again, then a third drug must be developed, and so on. For example, this has occurred for drugs used to treat gonorrhea infections. In the early 1940s, sulfa drugs were effective against gonorrhea. Resistance to sulfa drugs led to the use of penicillin, which was followed by ciprofloxacin (a quinolone), and finally ceftriaxone (a cephalosporin), the current drug of choice. |
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| beta-lactum antibacterials- list 3 |
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| Penicillins, Cephalosporin, Carbapenems |
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| Cephalosporin target what? |
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| Cephalosporins are the drug of choice for what bacteria? |
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| Neisseria infections (gonorrhea) |
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| Name an antibacterial that target cell membrane |
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| Name antibacterials that cause protein sythesis inhibition |
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Definition
| Aminoglycosides, Tetracyclines, Choramphenicol, Macrolides, |
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| Name antibacterials tha inhibit Nucleic acid synthesis |
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Definition
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| Name antibacterials that are Antimetabolites |
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Definition
| Sulfonamides,Isoniazid,Ethambutol |
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Definition
Imidazoles,Polyenes,Griseofulvin (Fulvicin), Flucytosine, Tolnaftate (Tinactin), Terbinafine (Lamisil)
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| Nucleotide analogs, Amantadine/Rimantadine, Oseltamivir (Tamiflu)/Zanamivir (Relenza),Interferons/Immunoenhancers |
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